Suchergebnisse

Context The cane toad (Rhinella marina), a native species of central and southern America, was introduced to Australia in 1935 as a biocontrol agent after a complex history of prior introductions. The population rapidly expanded and has since spread through much of the Australian landmass, with severe impacts on the endemic wildlife, primarily via toxicity to predators. The invasion process has taken its toll on the cane toad, with changes in the immunological capacity across the Australian invasive population. Aims To investigate the immunogenetic underpinnings of these changes, we studied the diversity of the Major Histocompatiblity Complex (MHC) genes in introduced cane toad populations. Methods We studied the diversity of two MHC genes (the classical class I UA locus and a class II DAB locus) and compared these with neutral microsatellite markers in toads from the Australian site of introduction and the Australian invasion front. We also included toads from Hawai'i, the original source of the Australian toads, to infer founder effect. Key results Diversity across all markers was low across Australian and Hawai'ian samples, consistent with a reduction in genetic diversity through multiple founder effects during the course of the successive translocations. In Australia, allelic diversity at the microsatellite markers and the UA locus was reduced at the invasion front, whereas all three alleles at the DAB locus were maintained in the invasion-front toads. Conclusions Loss of allelic diversity observed at the microsatellite markers and the UA locus could be the result of drift and bottlenecking along the invasion process, however, the persistence of DAB diversity warrants further investigation to disentangle the evolutionary forces influencing this locus. Implications Through the use of different molecular markers, we provide a preliminary description of the adaptive genetic processes occurring in this invasive population. The extremely limited MHC diversity may represent low immunogenetic competence across the Australian population, which could be exploited for invasive species management.

Immune-based fertility control is being considered as an effective long-term approach for controlling the pest brushtail possum (Trichosurus vulpecula) population in New Zealand. This relies heavily on the immune response of each immunised possum. A strong and lasting immune response in the majority of individuals in a population is essential. In this study, possums and the model macropod species, the tammar wallaby (Macropus eugenii) were immunised with either a luteinising hormone or androgen receptor synthetic peptide coupled to the carrier molecule KLH (keyhole limpet haemocyanin). The antibody response of wallabies to the antigens was relatively uniform. In contrast, the possum immunoglobulin response to both synthetic peptides and KLH was variable. The apparent high level of variation in the immune response of possums raises questions about the feasibility of using these two antigens to control possum numbers in New Zealand.

Globally, 15,521 animal species are listed as threatened by the International Union for the Conservation of Nature, and of these less than 3% have genomic resources that can inform conservation management. To combat this, global genome initiatives are developing genomic resources, yet production of a reference genome alone does not conserve a species. The reference genome allows us to develop a suite of tools to understand both genome-wide and functional diversity within and between species. Conservation practitioners can use these tools to inform their decision-making. But, at present there is an implementation gap between the release of genome information and the use of genomic data in applied conservation by conservation practitioners. In May 2020, we launched the Threatened Species Initiative and brought a consortium of genome biologists, population biologists, bioinformaticians, population geneticists, and ecologists together with conservation agencies across Australia, including government, zoos, and nongovernment organizations. Our objective is to create a foundation of genomic data to advance our understanding of key Australian threatened species, and ultimately empower conservation practitioners to access and apply genomic data to their decision-making processes through a web-based portal. Currently, we are developing genomic resources for 61 threatened species from a range of taxa, across Australia, with more than 130 collaborators from government, academia, and conservation organizations. Developed in direct consultation with government threatened-species managers and other conservation practitioners, herein we present our framework for meeting their needs and our systematic approach to integrating genomics into threatened species recovery.

Biodiversity conservation continually presents new challenges, yet conservation resources are limited, and funding for applied conservation re-search projects more so. Recently, many have reported on the "research–implementation gap," whereby conservation research findings are infrequently translated into conservation actions. In this perspective, we describe our experiences working in a large multi-institutional, multi-disciplinary team as we attempt to bridge the research–implementation gap by developing conservation tools needed to address the conservation challenges faced by Tasmanian devils (Sarcophilus harrisii). We discuss our project's history, lessons learnt,outcomes, and future plans to provide insights that may help others develop multi-institutional projects, designed to target rapid and direct implementation of conservation research into management action. Key to our success is the needs-based prioritization of research measured against the management team's questions, recognition of the different needs of academia, industry and government, a collegiate approach, and willingness to embrace adaptive management. Challenges include developing a project which meets all strategictargets of different institutions, in addition to sourcing funds. Overall, our goal has been to establish an enduring research-management framework, to facilitate improved integration of scientific research into the management needs of Tasmanian devil conservation, and serve as a template for other species management project

Devil facial tumor disease (DFTD) is renowned for its successful evasion of the host immune system. Down regulation of the major histocompatabilty complex class I molecule (MHC-I) on the DFTD cells is a primary mechanism of immune escape. Immunization trials on captive Tasmanian devils have previously demonstrated that an immune response against DFTD can be induced, and that immune-mediated tumor regression can occur. However, these trials were limited by their small sample sizes. Here, we describe the results of two DFTD immunization trials on cohorts of devils prior to their wild release as part of the Tasmanian Government's Wild Devil Recovery project. 95% of the devils developed anti-DFTD antibody responses. Given the relatively large sample sizes of the trials (N = 19 and N = 33), these responses are likely to reflect those of the general devil population. DFTD cells manipulated to express MHC-I were used as the antigenic basis of the immunizations in both trials. Although the adjuvant composition and number of immunizations differed between trials, similar anti-DFTD antibody levels were obtained. The first trial comprised DFTD cells and the adjuvant combination of ISCOMATRIX™, polyIC, and CpG with up to four immunizations given at monthly intervals. This compared to the second trial whereby two immunizations comprising DFTD cells and the adjuvant combination ISCOMATRIX™, polyICLC (Hiltonol®) and imiquimod were given a month apart, providing a shorter and, therefore, more practical protocol. Both trials incorporated a booster immunization given up to 5 months after the primary course. A key finding was that devils in the second trial responded more quickly and maintained their antibody levels for longer compared to devils in the first trial. The different adjuvant combination incorporating the RNAase resistant polyICLC and imiquimod used in the second trial is likely to be responsible. The seroconversion in the majority of devils in these anti-DFTD immunization trials was remarkable, especially as DFTD is ...

Devil facial tumor disease (DFTD) is renowned for its successful evasion of the host immune system. Down regulation of the major histocompatabilty complex class I molecule (MHC-I) on the DFTD cells is a primary mechanism of immune escape. Immunization trials on captive Tasmanian devils have previously demonstrated that an immune response against DFTD can be induced, and that immune-mediated tumor regression can occur. However, these trials were limited by their small sample sizes. Here, we describe the results of two DFTD immunization trials on cohorts of devils prior to their wild release as part of the Tasmanian Government's Wild Devil Recovery project. 95% of the devils developed anti-DFTD antibody responses. Given the relatively large sample sizes of the trials (N = 19 and N = 33), these responses are likely to reflect those of the general devil population. DFTD cells manipulated to express MHC-I were used as the antigenic basis of the immunizations in both trials. Although the adjuvant composition and number of immunizations differed between trials, similar anti-DFTD antibody levels were obtained. The first trial comprised DFTD cells and the adjuvant combination of ISCOMATRIX™, polyIC, and CpG with up to four immunizations given at monthly intervals. This compared to the second trial whereby two immunizations comprising DFTD cells and the adjuvant combination ISCOMATRIX™, polyICLC (Hiltonol®) and imiquimod were given a month apart, providing a shorter and, therefore, more practical protocol. Both trials incorporated a booster immunization given up to 5 months after the primary course. A key finding was that devils in the second trial responded more quickly and maintained their antibody levels for longer compared to devils in the first trial. The different adjuvant combination incorporating the RNAase resistant polyICLC and imiquimod used in the second trial is likely to be responsible. The seroconversion in the majority of devils in these anti-DFTD immunization trials was remarkable, especially as DFTD is hallmarked by its immune evasion mechanisms. Microsatellite analyzes of MHC revealed that some MHC-I microsatellites correlated to stronger immune responses. These trials signify the first step in the long-term objective of releasing devils with immunity to DFTD into the wild.